Kunes J, Zicha J
Institute of Physiology, Academy of Sciences of the Czech Republic, Prague.
Hypertension. 1994 Dec;24(6):645-7. doi: 10.1161/01.hyp.24.6.645.
Dietary sodium intake has long been considered an important factor in the genesis and maintenance of hypertension in both humans and experimental animals. To identify the possible association between salt sensitivity and genes of the major histocompatibility complex (RT1 complex), we studied the blood pressure response to an 8% NaCl diet in normotensive Lewis rats, spontaneously hypertensive rats (SHR), and Lewis.1K congenic rats (congenic to Lewis with the SHR main histocompatibility complex RT1). During the first 4 weeks of a high salt diet, the blood pressure increase was the same in SHR and Lewis.1K congenic rats. Thus, the presence of a small segment of SHR chromosome 20 with genes of the RT1 complex (and closely related genes) in the Lewis genome sensitized the blood pressure of these animals to the hypertensive effects of a high salt diet. Genes of the RT1 complex influenced the salt-induced increase of relative kidney weight more than that of relative heart weight. Our results support the hypothesis that some alleles within or close to the RT1 complex might be responsible for the higher sensitivity of hypertensive individuals to certain environmental stressors, including high salt intake.
长期以来，膳食钠摄入量一直被认为是人类和实验动物高血压发生和维持的一个重要因素。为了确定盐敏感性与主要组织相容性复合体（RT1复合体）基因之间的可能关联，我们研究了正常血压的Lewis大鼠、自发性高血压大鼠（SHR）和Lewis.1K同源近交系大鼠（与Lewis同源，具有SHR主要组织相容性复合体RT1）对8%氯化钠饮食的血压反应。在高盐饮食的前4周，SHR和Lewis.1K同源近交系大鼠的血压升高情况相同。因此，Lewis基因组中存在一小段带有RT1复合体基因（以及密切相关基因）的SHR 20号染色体，使这些动物的血压对高盐饮食的高血压效应敏感。RT1复合体基因对盐诱导的相对肾脏重量增加的影响大于对相对心脏重量增加的影响。我们的结果支持这样一种假设，即RT1复合体内或其附近的某些等位基因可能是高血压个体对某些环境应激源（包括高盐摄入）更高敏感性的原因。
